Acta Laser Biology Sinica, Volume. 31, Issue 5, 404(2022)

Effects of Aβ1-42 on the Expression and Electrophysiological Properties of Acid-sensing Ion Channel in Microglia

YU Xiaowei1,2、*, CAI Tuo2, ZHAN Lichao2, ZHU Xiaochuan2, YE Shengbao1, and GE Xingyi1
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  • 2[in Chinese]
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    References(25)

    [1] [1] GOEDERT M, SPILLANTINI M G, CAIRNS N J, et al. Tau proteins of Alzheimer paired helical filaments: abnormal phosphorylation of all six brain isoforms[J]. Neuron, 1992, 8(1): 159-168.

    [2] [2] ISING C, STANLEY M, HOLTZMAN D. Current thinking on the mechanistic basis of Alzheimer’s and implications for drug development[J]. Clinical Pharmacology and Therapeutics, 2015, 98(5): 469-471.

    [3] [3] SELKOE D J. The therapeutics of Alzheimer’s disease: where we stand and where we are heading[J]. Annals of Neurology, 2013, 74(3): 328-336.

    [4] [4] SEVIGNY J, CHIAO P, BUSSIERE T, et al. The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease[J]. Nature, 2016, 537(7618): 50-56.

    [5] [5] ABBOTT A, DOLGIN E. Failed Alzheimer’s trial does not kill leading theory of disease[J]. Nature, 2016, 540(7631): 15-16.

    [6] [6] PROKOP S, MILLER K R, HEPPNER F L. Microglia actions in Alzheimer’s disease[J]. Acta Neuropathologica, 2013, 126(4): 461-477.

    [7] [7] FU H, LIU B, FROST J L, et al. Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia[J]. Glia, 2012, 60(6): 993-1003.

    [8] [8] VARNUM M M, IKEZU T. The classification of microglial activation phenotypes on neurodegeneration and regeneration in Alzheimer’s disease brain[J]. Archivum Immunologiae et Therapiae Experimentalis, 2012, 60(4): 251-266.

    [9] [9] PAASILA P J, DAVIES D S, KRIL J J, et al. The relationship between the morphological subtypes of microglia and Alzheimer’s disease neuropathology[J]. Brain Pathology, 2019, 29(6): 726-740.

    [11] [11] STOROZHUKA M, CHERNINSKYIA A, MAXIMYUKA O, et al. Acid-sensing ion channels: focus on physiological and some pathological roles in the brain[J]. Current Neuropharmacology, 2021, 19(9): 1570-1589.

    [12] [12] SONDAG C M, DHAWAN G, COMBS C K. Beta amyloid oligomers and fibrils stimulate differential activation of primary microglia[J]. Journal of Neuroinflammation, 2009, 6(1): 1-13.

    [13] [13] NG J, KAUR H, COLLIER T, et al. Site-specific glycations of Aβ1-42 affect fibril formation and are neurotoxic[J]. Journal of Biological Chemistry, 2019, 294(22): 8806-8818.

    [14] [14] BUTTERFIELD D A, BOYD-KIMBALL D, PERRY G, et al. Oxidative stress, amyloid-β peptide, and altered key molecular pathways in the pathogenesis and progression of Alzheimer’s disease[J]. Journal of Alzheimer’s Disease, 2018, 62(3): 1345-1367.

    [15] [15] BENILOVA I, KARRAN E, STROOPER B D. The toxic Aβ oligomer and Alzheimer’s disease: an emperor in need of clothes[J]. Nature Neuroscience, 2012, 15(3): 349-357.

    [16] [16] CHENG Y, TIAN D Y, WANG Y J. Peripheral clearance of brain-derived Aβ in Alzheimer’s disease: pathophysiology and therapeutic perspectives[J]. Translational Neurodegeneration, 2020, 9(1): 16.

    [17] [17] TREMBLAY M E, STEVENS B, SIERRA A, et al. The role of microglia in the healthy brain[J]. Journal of Neuroscience, 2011, 31(45): 16064-16069.

    [18] [18] SARLUS H, HENEKA M T. Microglia in Alzheimer’s disease[J]. The Journal of Clinical Investigation, 2017, 127(9): 3240-3249.

    [20] [20] TOMUAR H, MOGI C, SATO K, et al. Proton-sensing and lysolipid-sensitive G-protein-coupled receptors: a novel type of multi-functional receptors[J]. Cellular Signalling, 2005, 17(12): 1466-1476.

    [21] [21] WEMMIE J A, CHEN J, ASKWITH C C, et al. The acid-activated ion channel ASIC contributes to synaptic plasticity, learning, and memory[J]. Neuron, 2002, 34(3): 463-477.

    [22] [22] CHU X P, XIONG Z G. Physiological and pathological functions of acid-sensing ion channels in the central nervous system[J]. Current Drug Targets, 2012, 13(2): 263-271.

    [23] [23] VERGO S, CRANER M J, ETZENSPERGER R, et al. Acid-sensing ion channel 1 is involved in both axonal injury and demyelination in multiple sclerosis and its animal model[J]. Brain, 2011, 134(Pt 2): 571-584.

    [24] [24] SUN X, CAO Y B, HU L F, et al. ASICs mediate the modulatory effect by paeoniflorin on α-synuclein autophagic degradation[J]. Brain Research, 2011, 1396: 77-87.

    [25] [25] YU X W, HU Z L, NI M, et al. Acid-sensing ion channels promote the inflammation and migration of cultured rat microglia[J]. Glia, 2015, 63(3): 483-496.

    [26] [26] HENEKA M T, KUMMER M P, STUTZ A, et al. NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice[J]. Nature, 2013, 493(7434): 674-678.

    [27] [27] HE P, ZHONG Z, KRISTINA L, et al. Deletion of tumor necrosis factor death receptor inhibits amyloid β generation and prevents learning and memory deficits in Alzheimer’s mice[J]. Journal of Cell Biology, 2007, 178(5): 829-841.

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    YU Xiaowei, CAI Tuo, ZHAN Lichao, ZHU Xiaochuan, YE Shengbao, GE Xingyi. Effects of Aβ1-42 on the Expression and Electrophysiological Properties of Acid-sensing Ion Channel in Microglia[J]. Acta Laser Biology Sinica, 2022, 31(5): 404

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    Paper Information

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    Received: Jun. 10, 2022

    Accepted: --

    Published Online: Jan. 18, 2023

    The Author Email: Xiaowei YU (yuxw0714@163.com)

    DOI:10.3969/j.issn.1007-7146.2022.05.004

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